A patient with acute coronary syndrome is treated with aspirin and what other class of medication to inhibit platelet aggregation?

In the context of treating acute coronary syndrome, the use of glycoprotein IIb/IIIa inhibitors is particularly important for their role in preventing platelet aggregation. In acute coronary syndromes, there is a substantial risk of thrombus formation due to platelet activation and aggregation. Glycoprotein IIb/IIIa inhibitors work by directly blocking the glycoprotein IIb/IIIa receptor on platelets, which is crucial for the binding of fibrinogen and subsequent platelet aggregation. This mechanism is vital in managing patients with unstable angina or those undergoing percutaneous coronary interventions (PCI), as it significantly reduces the risk of further thrombotic events.

While the other medications listed have important roles in the management of cardiovascular conditions, they do not serve the same purpose of directly inhibiting platelet aggregation. Beta-blockers primarily work to reduce heart rate and myocardial oxygen demand, ACE inhibitors are focused on lowering blood pressure and reducing ventricular remodeling after myocardial infarction, and calcium channel blockers help manage angina and hypertension but do not directly influence platelet function. Therefore, glycoprotein IIb/IIIa inhibitors are the appropriate choice to complement aspirin in preventing platelet-mediated thrombus formation during acute coronary syndrome.